The diagnosis and risk stratification of adverse events (death, heart attack, heart failure) in post-myocardial infarction patients have been described in conjunction with natriuretic proteins, namely, BNP and NTproBNP (Richards A. M., Nicholls M. G., Yandle T. O., Frampton C., Espiner E. A., Turner J. G., Buttimore R. C., Lainchbury J. G., Elliott J. M., Ikram H., Crozier I. G., Smyth D. W. Plasma N-terminal pro-brain natriuretic peptide and adrenomedullin: new neurohormonal predictors of left ventricular function and prognosis after myocardial infarction. Circulation 1998; 97:1921-1929; Squire I. B., O'Brien R. J., Demme B., Davies J. E., Ng L. L. N-terminal pro-atrial natriuretic peptide (N-ANP) and N-terminal pro-B-type natriuretic peptide (N-BNP) in the prediction of death and heart failure in unselected patients following acute myocardial infarction. Clin. Sci. (London) 2004; 107:309-316). However, it is particularly difficult to make a reliable diagnosis or to undertake a stratification in such post-myocardial infarction patients, especially as far as further clinical decisions are concerned.
Moreover, the state of the art describes pro-adrenomedullin (proADM) determination within the scope of the diagnosis (EP 0622458 B1), particularly for purposes of examining sepsis (EP 1121600 B1).
Circulating natriuretic peptide levels such as N-terminal pro B type natriuretic peptide (NTproBNP) provide prognostic information in patients at predicting death and heart failure in the post acute myocardial infarction (AMI) phase.1 The challenge remains to try and identify those patients who are deemed to be at high risk of adverse events. The addition of biomarkers in risk stratification has been shown to be superior to clinical features at predicting adverse outcomes and this has also been borne out in a range of acute coronary syndromes.2 Newer peptides are emerging which may give complementary and additional information, particularly in a multi-marker strategy with NTproBNP. Adrenomedullin (ADM) is a 52 amino acid peptide which has homology with calcitonin gene related peptide.3 It was originally isolated from human pheochromocytoma cells, however it has been detected in other tissues including adrenal medulla, heart, brain, lung, kidney, and gastrointestinal organs3,4 and its mRNA is highly expressed in endothelial cells.5 The downstream actions of ADM are mediated by an increase in cAMP levels.6 
ADM is synthesized as part of a larger precursor molecule, termed preproadrenomedullin. In humans this precursor consists of 185 amino acids.7 The gene encoding preproadrenomedullin is termed the ADM gene and has been mapped and localized to chromosome 11.8 ADM is difficult to measure in plasma as it can act in an autocrine or paracrine way, is partially complexed with complement factor H, and is rapidly cleared from the circulation.9 Recently, the more stable midregional fragment of pro-adrenomedullin (MR-proADM), comprising amino acids 45-92 of preproADM, has been identified which is more stable than the active molecule being secreted in equimolar amounts to adrenomedullin.10 
The biological activity of ADM in the cardiovascular system is similar to that of B-type natriuretic peptide (BNP) causing vasodilation11 via production of NO12 increasing cardiac output13 and inducing diuresis and natriuresis.14 Plasma ADM is increased in heart failure, in proportion to the severity of disease15,16 and is inversely related to LVEF.
Plasma ADM has been investigated previously in two small studies as a prognostic marker comparing it to NTproBNP and BNP.1,17 One study identified plasma ADM as an independent predictor of cardiogenic shock and short term mortality17, whereas ADM had no independent additional prognostic value to NTproBNP in another1.
It is an object of the present invention to provide an improved method for the diagnosis and risk stratification of adverse events in post-myocardial infarction patients.